RPI-1

• Catalog No.: R8907
• CAS Number: 269730-03-2
• M. F.: C17H15NO4
• M. W.: 297.3053
• Purity: ≥98% (HPLC)

SYNONYMS

• IUPAC name: 3-[(4-hydroxyphenyl)methylidene]-5,6-dimethoxy-2,3-dihydro-1H-indol-2-one
• IUPAC Traditional name: 3-[(4-hydroxyphenyl)methylidene]-5,6-dimethoxy-1H-indol-2-one
• Synonyms: 1,3-dihydro-5,6-dimethoxy-3-[(4-hydroxyphenyl)methylene]-H-indol-2-one

DATABASE IDS

• CAS Number: 269730-03-2
• MDL Number: MFCD03852474

PROPERTIES

• Empirical Formula (Hill Notation): C17H15NO4
• Purity: ≥98% (HPLC)
• Apperance: orange powder
• Solubility: DMSO: >20 mg/mL
• GHS Signal Word: Warning
• GHS Hazard statements: H400
• European Hazard Symbols: Nature polluting (N)
• Personal Protective Equipment: dust mask type N95 (US), Eyeshields, Gloves
• GHS Precautionary statements: P273
• Risk Statements: 50/53
• Safety Statements: 60-61
• Storage Temperature: 2-8°C
• German water hazard class: 3

DETAILS

Description (English)

Biochem/physiol Actions
RPI-1 is a competitive, potent ATP-dependent Ret kinase inhibitor. Recently it was discover that the compound also inhibits c-Met. Increased tumorigenicity, motility, and invasiveness have been described as biological consequences of HGF/Met deregulation in tumor cells, thus not surprisingly RPI-1 treatment of H460 cells resulted in a strong reduction of both colony number and size (IC50 = 24.5 + 0.5 microM). Compound is also active at mouse NSCLC H460 xenograft tumor and metastasis model. Mechanistically RPI-1 inhibits Met phosphorylation at Tyr1234/Tyr1235, known to activate the intrinsic kinase activity. It appears that " Ret/ptc1 cross talks with Met at transcriptional and signaling levels and promotes ?-catenin transcriptional activity to drive thyrocyte neoplastic transformation". It appears that we do not have anything specific in Ret area. Handbook lists RPI-1 as Ret inhibitor.

Description (简体中文)

Biochem/physiol Actions
RPI-1 is a competitive, potent ATP-dependent Ret kinase inhibitor. Recently it was discover that the compound also inhibits c-Met. Increased tumorigenicity, motility, and invasiveness have been described as biological consequences of HGF/Met deregulation in tumor cells, thus not surprisingly RPI-1 treatment of H460 cells resulted in a strong reduction of both colony number and size (IC50 = 24.5 + 0.5 microM). Compound is also active at mouse NSCLC H460 xenograft tumor and metastasis model. Mechanistically RPI-1 inhibits Met phosphorylation at Tyr1234/Tyr1235, known to activate the intrinsic kinase activity. It appears that " Ret/ptc1 cross talks with Met at transcriptional and signaling levels and promotes ?-catenin transcriptional activity to drive thyrocyte neoplastic transformation". It appears that we do not have anything specific in Ret area. Handbook lists RPI-1 as Ret inhibitor.